|1.||Saito, H: 3 articles (08/2002 - 03/2000)|
|2.||Naoe, T: 3 articles (08/2002 - 03/2000)|
|3.||Yamamoto, Y: 3 articles (08/2002 - 03/2000)|
|4.||Ueda, R: 3 articles (08/2002 - 03/2000)|
|5.||Minami, Y: 2 articles (08/2002 - 08/2001)|
|6.||Kiyoi, H: 2 articles (08/2002 - 03/2000)|
|7.||Yamamoto, K: 2 articles (08/2002 - 08/2001)|
|8.||Heikkila, John J: 1 article (10/2008)|
|9.||Voyer, Janine: 1 article (10/2008)|
|10.||Queiroz, C M: 1 article (05/2008)|
12/19/2003 - "Herbimycin A induces sympathetic neuron survival and protects against hypoxia."
03/01/2003 - "The herbimycin A-induced increase in HSP-70i protected cells from hypoxia injury."
12/19/2003 - "In the presence of NGF and 100 ng/ml herbimycin, 81% of the neurons survived hypoxia. "
06/01/1995 - "These results suggest that PKC and herbimycin-sensitive tyrosine kinase may serve as negative regulators of the hypoxia-activated signal transduction pathway that leads to the induction of VEGF expression. "
06/01/1995 - "Furthermore, chronic exposure to TPA or treatment with herbimycin A results in the enhancement of the hypoxia-mediated increase in VEGF mRNA levels. "
11/01/1994 - "injection inhibited tumor formation and significantly prolonged survival time, and further, in mice inoculated with 1 x 10(4) cells, herbimycin A completely suppressed the in vivo growth of transformant FDC-P2 cells and brought about a complete remission. "
08/01/2007 - "As expected, herbimycin A treatment reduced tumor growth as assessed both by tumor volume measurement and bioluminescent imaging. "
07/01/1996 - "During 2-day treatment with herbimycin A, no changes were observed in tumor size. "
09/01/1989 - "We have examined the suppressive effect of herbimycin A on the reduction of gap-junctional intercellular communication that is induced by a tumor-promoting phorbol ester in 3T3-L1 cells. "
09/01/1989 - "Herbimycin A suppresses the reduction of gap-junctional intercellular communication induced by tumor-promoting phorbol ester in 3T3-L1 cells."
09/01/1992 - "The present study indicates that herbimycin A is a beneficial agent for the investigation of the role of the bcr-abl gene in Ph1-positive leukemias and further suggests that the development of agents inhibiting the bcr-abl gene product may offer a new therapeutic potential for Ph1-positive leukemias."
08/01/2002 - "As a therapeutic approach, we previously reported that herbimycin A (HA) inhibited the growth of tandemly duplicated FLT3 (TDFLT3)-transformed cells (Leukemia 2000; 14: 374). "
08/01/2001 - "In mice transplanted with transformed 32D cells, the administration of herbimycin A completely prevented leukemia progression. "
03/01/2000 - "In mice transplanted with the transformed 32D cells, the administration of herbimycin A prolonged the latency of disease or completely prevented leukemia, depending on the number of cells inoculated and schedule of drug administration. "
03/01/1994 - "Herbimycin A, a benzoquinonoid anasamycin antibiotic, preferentially inhibited the in vitro growth of Ph1-positive leukemia cell lines. "
04/01/2000 - "Binding of the heat shock factor (HSF) to the heat shock element (HSE) in the presence of herbimycin A or delta12PGJ2, and the effects of DTT, mirrored the results of Hsp70 induction. "
01/01/1997 - "Enhanced synthesis of a 34-kDa protein appears to be specific to herbimycin A because its synthesis did not increase after heat shock (35 degrees C). "
03/01/2003 - "Herbimycin A induced the phosphorylation of heat shock factor 1 (HSF1), while genistein reduced HSF1 production. "
01/01/2003 - "Stress proteins were induced 18 h pre-operatively by heat shock or herbimycin A. "
01/01/1997 - "Finally, concurrent treatment of cells with 0.5 microgram/mL herbimycin A and a mild heat shock of 27 degrees C yielded a synergistic accumulation of hsp30 and hsp70 mRNA. "
|1.||Protein-Tyrosine Kinases (Tyrosine Kinase)
|8.||Messenger RNA (mRNA)
|9.||Anti-Bacterial Agents (Antibiotics)
|10.||Staphylococcal Protein A (A, Protein)